Lactobacillus rhamnosus RC007 intended for feed additive: immune-stimulatory properties and ameliorating effects on TNBS-induced colitis

2016 ◽  
Vol 7 (4) ◽  
pp. 539-547 ◽  
Author(s):  
C. Dogi ◽  
G. García ◽  
A. De Moreno de LeBlanc ◽  
C. Greco ◽  
L. Cavaglieri
Keyword(s):  
Intestinal Inflammation ◽  
Animal Feed ◽  
Lactobacillus Rhamnosus ◽  
Feed Additive ◽  
Necrosis Factor Alpha ◽  
Benzene Sulfonic Acid ◽  
Therapeutic Benefits ◽  
Tnf Α ◽  
Intestinal Fluids ◽  
Healthy Host

Lactobacillus rhamnosus RC007 is a potential probiotic bacterium that can exert beneficial effects as supplement for animal feed, by improving the immune status in healthy host, and by providing therapeutic benefits to infected/inflamed animals. The aim of the present work was to evaluate in vivo the beneficial properties of L. rhamnosus RC007, intended for animal feed, when administered to healthy and trinitro-benzene-sulfonic-acid (TNBS) colitis induced BALB/c mice. The administration of L. rhamnosus RC007 to healthy mice during 10 days increased the phagocytic activity of peritoneal macrophages and the number of immunoglobulin A+ cells in the lamina proper of the small intestine. Significant increases of monocyte chemotactic protein 1, interleukin (IL)-10 and tumour necrosis factor alpha (TNF-α) concentrations, and in the ratio between anti- and pro-inflammatory cytokines (IL-10/TNF-α) were observed in intestinal fluids after administration of bacteria. In the inflammation model, less body weight loss, macroscopic and histological damages in the large intestine were accompanied by increased IL-10/TNF-α ratio in the intestinal fluids of mice from the L. rhamnosus-TNBS group when compared to the TNBS group. In a healthy host, the oral administration of L. rhamnosus RC007 kept the gut immune system stimulated allowing a faster response to noxious stimulus. Mice that received L. rhamnosus RC007 also decreased the severity of the intestinal inflammation.

scholarly journals Fidaxomicin and OP-1118 Inhibit Clostridium difficile Toxin A- and B-Mediated Inflammatory Responses via Inhibition of NF-κB Activity

2017 ◽  
Vol 62 (1) ◽  
Author(s):  
Hon Wai Koon ◽  
Jiani Wang ◽  
Caroline C. Mussatto ◽  
Christina Ortiz ◽  
Elaine C. Lee ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Human Colon ◽  
Toxin A ◽  
Primary Metabolite ◽  
Necrosis Factor Alpha ◽  
Toxin B ◽  
Content Type ◽  
Tnf Α

ABSTRACTClostridium difficilecauses diarrhea and colitis by releasing toxin A and toxin B. In the human colon, both toxins cause intestinal inflammation and stimulate tumor necrosis factor alpha (TNF-α) expression via the activation of NF-κB. It is well established that the macrolide antibiotic fidaxomicin is associated with reduced relapses ofC. difficileinfection. We showed that fidaxomicin and its primary metabolite OP-1118 significantly inhibited toxin A-mediated intestinal inflammation in micein vivoand toxin A-induced cell roundingin vitro. We aim to determine whether fidaxomicin and OP-1118 possess anti-inflammatory effects against toxin A and toxin B in the human colon and examine the mechanism of this response. We used fresh human colonic explants, NCM460 human colonic epithelial cells, and RAW264.7 mouse macrophages to study the mechanism of the activity of fidaxomicin and OP-1118 against toxin A- and B-mediated cytokine expression and apoptosis. Fidaxomicin and OP-1118 dose-dependently inhibited toxin A- and B-induced TNF-α and interleukin-1β (IL-1β) mRNA expression and histological damage in human colonic explants. Fidaxomicin and OP-1118 inhibited toxin A-mediated NF-κB phosphorylation in human and mouse intestinal mucosae. Fidaxomicin and OP-1118 also inhibited toxin A-mediated NF-κB phosphorylation and TNF-α expression in macrophages, which was reversed by the NF-κB activator phorbol myristate acetate (PMA). Fidaxomicin and OP-1118 prevented toxin A- and B-mediated apoptosis in NCM460 cells, which was reversed by the addition of PMA. PMA reversed the cytoprotective effect of fidaxomicin and OP-1118 in toxin-exposed human colonic explants. Fidaxomicin and OP-1118 inhibitC. difficiletoxin A- and B-mediated inflammatory responses, NF-κB phosphorylation, and tissue damage in the human colon.

scholarly journals Impact of dietary Mannan-oligosaccharide and β-Glucan supplementation on growth, histopathology, E-coli colonization and hepatic transcripts of TNF-α and NF- ϰB of broiler challenged with E. coli O78

2020 ◽  
Author(s):  
Sabreen Ezzat Fadl ◽  
Ghada Ahmed El-Gammal ◽  
Osama Atia Sakr ◽  
Aly A.B.S. Salah ◽  
Ayman Ali Atia ◽  
...  
Keyword(s):  
Growth Performance ◽  
Animal Feed ◽  
Serum Biochemistry ◽  
Growth Promoters ◽  
Necrosis Factor Alpha ◽  
Mannan Oligosaccharide ◽  
E Coli ◽  
Tnf Α ◽  
Liver Gene ◽  
The Impact

Abstract Background: Using probiotics have become popular. They are considered an alternative to Antibiotic Growth Promoters (AGP). Probiotics are supplemented into animal feed for improving growth performance along with preventing and controlling enteric pathogens. The aim of this work was to study the impact of dietary supplementation of Mannan-oligosaccharide and β-Glucan (Agrimos®) on broiler challenged with Escherichia coli O78 (E. coli O78 - marked with an antibiotic (320 μg ciprofloxacin/ml broth) on growth performance, serum biochemistry, immune organs-histopathology, E-coli colonization, and hepatic transcripts of Tumor necrosis factor-alpha (TNF-α) and Nuclear factor-kappa B (NF-ϰB).Methods: A total of 125 one-day-old chicks were used for conducting the experiment. Five one-day-old chicks were slaughtered for measuring the initial weight of lymphoid tissue. The remaining chicks (120) were allotted into four groups according to Mannan-oligosaccharide and β-Glucan supplementation and E. coli infection. The data were analyzed using SPSS version 16.Results: Results indicated significant alteration of growth performance, serum biochemistry, selected liver gene expression with pathological lesions especially in lymphoid organs due to E. coli infection. These alterations were mitigated by Mannan-oligosaccharide and β-Glucan supplementation.Conclusion: It could be concluded Mannan-oligosaccharide and β-Glucan supplementation in broiler's diet improved the immune response of broilers and mitigated pathological lesion resulted from E. coli infection.

scholarly journals Prohibitin Inhibits Tumor Necrosis Factor alpha–induced Nuclear Factor-kappa B Nuclear Translocation via the Novel Mechanism of Decreasing Importin α3 Expression

2009 ◽  
Vol 20 (20) ◽  
pp. 4412-4423 ◽  
Author(s):  
Arianne L. Theiss ◽  
Aaron K. Jenkins ◽  
Ngozi I. Okoro ◽  
Jan-Michael A. Klapproth ◽  
Didier Merlin ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Inflammation ◽  
Nuclear Translocation ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha

Expression of prohibitin 1 (PHB), a multifunctional protein in the cell, is decreased during inflammatory bowel disease (IBD). Little is known regarding the regulation and role of PHB during intestinal inflammation. We examined the effect of tumor necrosis factor alpha (TNF-α), a cytokine that plays a central role in the pathogenesis of IBD, on PHB expression and the effect of sustained PHB expression on TNF-α activation of nuclear factor-kappa B (NF-κB) and epithelial barrier dysfunction, two hallmarks of intestinal inflammation. We show that TNF-α decreased PHB protein and mRNA abundance in intestinal epithelial cells in vitro and in colon mucosa in vivo. Sustained expression of prohibitin in intestinal epithelial cells in vitro and in vivo (prohibitin transgenic mice, PHB TG) resulted in a marked decrease in TNF-α–induced nuclear translocation of the NF-κB protein p65, NF-κB/DNA binding, and NF-κB–mediated transcriptional activation despite robust IκB-α phosphorylation and degradation and increased cytosolic p65. Cells overexpressing PHB were protected from TNF-α–induced increased epithelial permeability. Expression of importin α3, a protein involved in p50/p65 nuclear import, was decreased in cells overexpressing PHB and in colon mucosa of PHB TG mice. Restoration of importin α3 levels sustained NF-κB activation by TNF-α during PHB transfection. These results suggest that PHB inhibits NF-κB nuclear translocation via a novel mechanism involving alteration of importin α3 levels. TNF-α decreases PHB expression in intestinal epithelial cells and restoration of PHB expression in these cells can protect against the deleterious effects of TNF-α and NF-κB on barrier function.

scholarly journals Impact of dietary Mannan-oligosaccharide and β-Glucan supplementation on growth, histopathology, E-coli colonization and hepatic transcripts of TNF-α and NF- ϰB of broiler challenged with E. coli O78

2019 ◽  
Author(s):  
Sabreen Ezzat Fadl ◽  
Ghada Ahmed El-Gammal ◽  
Osama Atia Sakr ◽  
Abdelbary Mohammed Prince ◽  
Aly A.B.S. Salah ◽  
...  
Keyword(s):  
Growth Performance ◽  
Animal Feed ◽  
Serum Biochemistry ◽  
Growth Promoters ◽  
Necrosis Factor Alpha ◽  
Mannan Oligosaccharide ◽  
E Coli ◽  
Tnf Α ◽  
Liver Gene ◽  
The Impact

Abstract Background: Using probiotics have become popular. They are considered an alternative to Antibiotic Growth Promoters (AGP). Probiotics are supplemented into animal feed for improving growth performance along with preventing and controlling enteric pathogens. The aim of this work was to study the impact of dietary supplementation of Mannan-oligosaccharide and β-Glucan (Agrimos®) on broiler challenged with Escherichia coli O78 (E. coli O78 - marked with an antibiotic (320 μg ciprofloxacin/ml broth) on growth performance, serum biochemistry, immune organs-histopathology, E-coli colonization, and hepatic transcripts of Tumor necrosis factor-alpha (TNF-α) and Nuclear factor-kappa B (NF-ϰB). Methods: A total of 125 one-day-old chicks were used for conducting the experiment. Five chicks were slaughtered for measuring the initial weight of lymphoid tissue; the remaining chicks (120) were allotted into four groups according to Mannan-oligosaccharide and β-Glucan supplementation and E. coli infection. The data were analyzed using SPSS version 16. Results: Results indicated significant alteration of growth performance, serum biochemistry, selected liver gene expression with pathological lesions, especially in lymphoid organs due to E. coli infection, which were mitigated by Mannan-oligosaccharide and β-Glucan supplementation. Conclusion: It could be concluded Mannan-oligosaccharide and β-Glucan supplementation in broiler's diet improved the immune response of broilers and mitigated pathological lesion resulted from E. coli infection.

scholarly journals Topical Therapy with Antisense Tumor Necrosis Factor Alpha Using Novel β-Glucan-Based Drug Delivery System Ameliorates Intestinal Inflammation

2020 ◽  
Vol 21 (2) ◽  
pp. 683 ◽  
Author(s):  
Hideto Sakisaka ◽  
Hidetoshi Takedatsu ◽  
Keiichi Mitsuyama ◽  
Shinichi Mochizuki ◽  
Kazuo Sakurai ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Delivery System ◽  
Therapeutic Efficacy ◽  
Tumor Necrosis ◽  
Intestinal Inflammation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Anti-tumor necrosis factor alpha (TNF-α) antibodies are effective in patients with inflammatory bowel disease (IBD). However, the effect is not optimal because a sufficient concentration of antibodies cannot be maintained at the site of inflammation. Thus, a macromolecular complex was developed with schizophyllan (SPG) and antisense oligonucleotides. In the present study, an SPG-antisense TNF-α complex was prepared, and its therapeutic efficacy was examined using a dextran sodium sulfate (DSS)-induced colitis model. The TNF-α production in CD11b+ macrophages significantly increased in the colon of DSS-treated mice. Dectin-1, a receptor of SPG, binds with SPG and is subsequently taken into the cells via phagocytosis. The expression of dectin-1 by CD11b+ macrophages significantly increased in DSS-treated mice. Flow cytometry revealed that the uptake of SPG-antisense TNF-α in the macrophages was efficient. TNF-α production was suppressed significantly by SPG-antisense TNF-α in vitro, which was administered via enema to evaluate its efficacy. The intrarectal administration of SPG-antisense TNF-α ameliorated the intestinal inflammation. In this study, we showed that the delivery system that conjugates SPG and antisense can have higher therapeutic efficacy. Thus, the new therapeutic approach presented in this study may be used in the management of IBD.

scholarly journals Lactobacillus rhamnosus GG Derived Extracellular Vesicles Modulate Gut Microbiota and Attenuate Inflammatory in DSS-Induced Colitis Mice

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3319
Author(s):  
Lingjun Tong ◽  
Xinyi Zhang ◽  
Haining Hao ◽  
Qiqi Liu ◽  
Zihan Zhou ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Extracellular Vesicles ◽  
Intestinal Inflammation ◽  
Lactobacillus Rhamnosus ◽  
Underlying Mechanism ◽  
Lactobacillus Rhamnosus Gg ◽  
Tnf Α ◽  
Rrna Sequencing ◽  
Clinical Benefits ◽  
Pro Inflammatory Cytokines

Ulcerative colitis (UC) is a relapsing and remitting inflammatory disease. Probiotics have a potential beneficial effect on the prevention of UC onset and relapse in clinical trials. Lactobacillus rhamnosus GG (L. rhamnosus GG) have shown clinical benefits on UC patients, however, the precise mechanisms are unknown. The aim of this study is to explore the effect of extracellular vesicles released from L. rhamnosus GG (LGG-EVs) on dextran sulfate sodium (DSS)-induced colitis and propose the underlying mechanism of LGG-EVs for protecting against colitis. The results showed that LGG-EVs could prevent colonic tissue damage and shortening of the colon (p < 0.01), and ameliorate intestinal inflammation by inhibiting TLR4-NF-κB-NLRP3 axis activation. Consistently, the pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-2) were suppressed effectively upon LGG-EVs treatment (p < 0.05). The 16S rRNA sequencing showed that LGG-EVs administration could reshape the gut microbiota in DSS-induced colitis mice, which further alters the metabolism pathways of gut microbiota. These findings propose a novel perspective of L. rhamnosus GG in attenuating inflammation mediated by extracellular vesicles and offer consideration for developing oral gavage of LGG-EVs for colitis therapies.

scholarly journals Effect of Escherichia coli and Lactobacillus rhamnosus on Macrophage Inflammatory Protein 3α, Tumor Necrosis Factor Alpha, and Transforming Growth Factor β Release by Polarized Rat Uterine Epithelial Cells in Culture

2004 ◽  
Vol 72 (4) ◽  
pp. 1866-1873 ◽  
Author(s):  
Mardi A. Crane-Godreau ◽  
Charles R. Wira
Keyword(s):  
Epithelial Cell ◽  
Transforming Growth Factor ◽  
Lactobacillus Rhamnosus ◽  
Transforming Growth Factor Β ◽  
Necrosis Factor Alpha ◽  
E Coli ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Entry of bacteria from the vagina into the uterus raises the question of uterine epithelial cell (UEC) signaling in response to the presence of bacteria. Our model system helps to define microbially elicited UEC basolateral cytokine release, important in regulating underlying stromal immune cell protection. UECs from adult rats were grown in cell culture inserts to establish a confluent polarized monolayer as was determined by transepithelial resistance (TER). Polarized epithelial cell cultures were treated apically with live or heat-killed Escherichia coli or Lactobacillus rhamnosus prior to collection of basolateral media after 24 h of incubation. Coculture of polarized UECs with live E. coli had no effect on epithelial cell TER. In response to exposure to live E. coli, epithelial cell basolateral release of macrophage inflammatory protein 3α (MIP3α) and tumor necrosis factor alpha (TNF-α) increased at a time when basolateral release of biologically active transforming growth factor β (TGF-β) decreased. Incubation of UECs with heat-killed E. coli resulted in an increased basolateral release of MIP3α and TNF-α, without affecting TER or TGF-β. In contrast to E. coli, live or heat-killed L. rhamnosus had no effect on TER or cytokine release. These studies indicate that polarized rat UECs respond to gram-negative E. coli by releasing the cytokines MIP3α and TNF-α, signals important to both the innate and adaptive immune systems. These findings suggest that UEC responses to bacteria are selective and important in initiating and regulating immune protection in the female reproductive tract.

scholarly journals TPL2 Is a Key Regulator of Intestinal Inflammation in Clostridium difficile Infection

2018 ◽  
Vol 86 (8) ◽  
Author(s):  
Yuanguo Wang ◽  
Shaohui Wang ◽  
Ciaran P. Kelly ◽  
Hanping Feng ◽  
Andrew Greenberg ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Specific Inhibitor ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Gene Ablation ◽  
Extracellular Signal ◽  
Tnf Α ◽  
Mitogen Activated Protein

ABSTRACT Tumor progression locus 2 (TPL2), a serine/threonine protein kinase, is a major inflammatory mediator in immune cells. The predominant inflammatory actions of TPL2 depend on the activation of mitogen-activated protein kinases (MAPK) and the upregulated production of the cytokines tumor necrosis factor alpha (TNF-α) and interleukin 1β (IL-1β) in macrophages and dendritic cells in response to lipopolysaccharide (LPS). Significant increases in TNF-α, IL-6, IL-β, and IL-8 levels in patients with Clostridium difficile infection (CDI) have been reported. Both TNF-α and IL-6 have been postulated to play key roles in the systemic inflammatory response in CDI, and IL-8 is essential for the development of local intestinal inflammatory responses in CDI. The objective of this study was to elucidate the role of TPL2 in the pathogenesis of CDI. We found that TPL2 was significantly activated in human and mouse intestinal tissues upon C. difficile toxin exposure or CDI. We further demonstrated that TPL2 knockout (TPL2-KO) mice were significantly more resistant to CDI than wild-type mice, with significantly reduced production of TNF-α, IL-6, IL-1β, KC (a mouse homologue of IL-8), and myeloperoxidase (MPO) in the ceca and colons of TPL2-KO mice. Finally, we found that TPL2 inhibition by a specific inhibitor or TPL2 gene ablation significantly reduced TcdB-induced production of TNF-α, IL-6, IL-β, and KC by inhibiting the activation of p38, extracellular signal-regulated kinase (ERK), and c-Jun NH2-terminal kinase (JNK). Taken together, our data suggest that TPL2 represents a potential therapeutic target for CDI treatment.

scholarly journals Complexity of TNF-α Signaling in Heart Disease

2020 ◽  
Vol 9 (10) ◽  
pp. 3267
Author(s):  
Filip Rolski ◽  
Przemysław Błyszczuk
Keyword(s):  
Heart Disease ◽  
Molecular Mechanisms ◽  
Treatment Options ◽  
Cell Types ◽  
Published Data ◽  
Necrosis Factor Alpha ◽  
Failing Heart ◽  
Therapeutic Benefits ◽  
Tnf Α

Heart disease is a leading cause of death with unmet clinical needs for targeted treatment options. Tumor necrosis factor alpha (TNF-α) represents a master pro-inflammatory cytokine that plays an important role in many immunopathogenic processes. Anti-TNF-α therapy is widely used in treating autoimmune inflammatory disorders, but in case of patients with heart disease, this treatment was unsuccessful or even harmful. The underlying reasons remain elusive until today. This review summarizes the effects of anti-TNF-α treatment in patients with and without heart disease and describes the involvement of TNF-α signaling in a number of animal models of cardiovascular diseases. We specifically focused on the role of TNF-α in specific cardiovascular conditions and in defined cardiac cell types. Although some mechanisms, mainly in disease development, are quite well known, a comprehensive understanding of TNF-α signaling in the failing heart is still incomplete. Published data identify pathogenic and cardioprotective mechanisms of TNF-α in the affected heart and highlight the differential role of two TNF-α receptors pointing to the complexity of the TNF-α signaling. In the light of these findings, it seems that targeting the TNF-α pathway in heart disease may show therapeutic benefits, but this approach must be more specific and selectively block pathogenic mechanisms. To this aim, more research is needed to better understand the molecular mechanisms of TNF-α signaling in the failing heart.

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